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mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution

View ORCID ProfileChristopher M. Weber, View ORCID ProfileAntonina Hafner, Simon M. G. Braun, View ORCID ProfileJacob G. Kirkland, View ORCID ProfileBenjamin Z. Stanton, View ORCID ProfileAlistair N. Boettiger, Gerald R. Crabtree
doi: https://doi.org/10.1101/2020.01.29.925586
Christopher M. Weber
1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
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Antonina Hafner
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
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  • ORCID record for Antonina Hafner
Simon M. G. Braun
1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
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Jacob G. Kirkland
1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
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Benjamin Z. Stanton
3Nationwide Children’s Hospital, Center for Childhood Cancer and Blood Diseases, Columbus, Ohio, USA
4Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA
5Department of Biological Chemistry and Pharmacology, The Ohio State University College of Medicine, Columbus, Ohio, USA
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Alistair N. Boettiger
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
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Gerald R. Crabtree
1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
6Howard Hughes Medical Institute, Chevy Chase, Maryland, USA
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  • For correspondence: crabtree@stanford.edu
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Abstract

The mammalian SWI/SNF, or BAF complex, has a conserved and direct role in antagonizing polycomb-mediated repression. Yet, BAF appears to also promote repression by polycomb in stem cells and cancer. How BAF both antagonizes and promotes polycomb-mediated repression remains unknown. Here, we utilize targeted protein degradation to dissect the BAF-polycomb axis in embryonic stem cells on the timescale of hours. We report that rapid BAF depletion redistributes both PRC1 and PRC2 complexes from highly occupied domains, like Hox clusters, to weakly occupied sites that are normally opposed by BAF. Polycomb redistribution from highly repressed domains results in their decompaction, gain of active epigenomic features, and transcriptional derepression. Surprisingly, through dose-dependent degradation of PRC1 & PRC2 we identify both a conventional role for BAF in polycomb-mediated repression and a second mechanism acting by global redistribution of polycomb. These findings provide new mechanistic insight into the highly dynamic state of the Polycomb-Trithorax axis.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted December 07, 2020.
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mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution
Christopher M. Weber, Antonina Hafner, Simon M. G. Braun, Jacob G. Kirkland, Benjamin Z. Stanton, Alistair N. Boettiger, Gerald R. Crabtree
bioRxiv 2020.01.29.925586; doi: https://doi.org/10.1101/2020.01.29.925586
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mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution
Christopher M. Weber, Antonina Hafner, Simon M. G. Braun, Jacob G. Kirkland, Benjamin Z. Stanton, Alistair N. Boettiger, Gerald R. Crabtree
bioRxiv 2020.01.29.925586; doi: https://doi.org/10.1101/2020.01.29.925586

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